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首页> 外文期刊>Environmental research >Risk of occupational exposure to asbestos, silicon and arsenic on pulmonary disorders: Understanding the genetic-epigenetic interplay and future prospects
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Risk of occupational exposure to asbestos, silicon and arsenic on pulmonary disorders: Understanding the genetic-epigenetic interplay and future prospects

机译：在肺部疾病中职业性接触石棉，硅和砷的风险：了解遗传表观遗传相互作用和未来前景

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Background: Epidemiological studies suggest strong association of lung disorders with occupational exposure to asbestos, silicon and arsenic. The chronic occupational exposure primarily through inhalation results in adverse outcome on the respiratory tract which may also be fatal. Although several mechanisms have attributed towards these diseases; the molecular pathogenesis is still unknown. Objective: In this review, we investigated the plausible molecular mechanism based on current research that may identify the genetic and epigenetic susceptibility of respiratory disorders upon such occupational exposures in humans. Methods: We considered genetic variants and epigenetic alterations associated with pulmonary exposure hazards leading to asbestosis, silicosis and arsenicosis. Our review is stringently based on the literatures available through peer-reviewed articles mostly published in the last 10 years. Relevant search were conducted using keywords like "occupational lung disorders" along with "asbestos", "silicon" and "arsenic". Results: Till September 2015, pubmed search yielded approximately 780 articles relating to asbestos exposure; 240 articles for silicon exposure and 60 articles for arsenic exposure. Extensive screening for genetic and epigenetic factors identified certain genes and related pathways that are important to determine the susceptibility of an individual towards such occupational exposure. Conclusion: The link between genotype and phenotype and its association with disease susceptibility is very complex in nature due to several factors like person's environment, lifestyle and nutritional status. The epigenome is dynamic as well as reversible and can be reshaped further by certain dietary components throughout its life. In the present review, we have addressed the role of molecular pathogenesis of occupational lung diseases based on the genetic variability and epigenetic alterations and also attempted to highlight the promising aspect of dietary interventions to counter toxic outcomes upon occupational exposure to asbestos, silicon or arsenic.
机译：背景：流行病学研究表明，肺部疾病与职业性接触石棉，硅和砷有很强的联系。慢性职业暴露主要通过吸入导致呼吸道不良后果，这也可能是致命的。尽管有几种机制可归因于这些疾病。分子发病机制仍然未知。目的：在这篇综述中，我们基于当前的研究调查了可能的分子机制，该机制可能确定了人类在这种职业暴露下呼吸系统疾病的遗传和表观遗传易感性。方法：我们考虑了遗传变异和表观遗传改变，这些变异与导致石棉沉滞，矽肺和砷中毒的肺部暴露危险有关。我们的审查严格基于过去十年中发表的大多数同行评审文章中提供的文献。使用诸如“职业性肺部疾病”以及“石棉”，“硅”和“砷”之类的关键词进行相关搜索。结果：截至2015年9月，公开搜索共发表了约780篇与石棉接触有关的文章。硅暴露量为240，砷暴露量为60。对遗传和表观遗传因素的广泛筛选确定了某些基因和相关途径，这些对于确定个人对这种职业暴露的敏感性很重要。结论：由于人的环境，生活方式和营养状况等多种因素，基因型与表型之间的联系及其与疾病易感性的联系在本质上非常复杂。表观基因组既动态又可逆，可以在其一生中通过某些饮食成分进一步重塑。在本综述中，我们基于遗传变异性和表观遗传学改变，探讨了职业性肺病分子发病机理的作用，并试图强调饮食干预措施有前景的方面，以应对职业性接触石棉，硅或砷的毒性结果。

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